Lossofgastriccontentsfromthebody(e.g.,vomiting,nasogastricsuctioning)producesmetabolicalkalosissecondarytothelossofHCl.Ifthelossofgastricfluidissignificant,ECFVcontractionoccurs.UnderthisconditionthekidneyscannotexcretesufficientquantitiesofHCO3− tocompensateforthemetabolicalkalosis.TheinabilityofthekidneystoexcreteHCO3− isaresultoftheneedtoreduceNa+ excretiontocorrecttheECFVcontraction.Asdescribedpreviously(see fordetails)theresponseofthekidneystovolumecontractionistoreducetheglomerularfiltrationrate,whichreducesthefilteredloadofHCO3− ,andtoincreaseNa+ reabsorptionalongthenephron.BecausealargeamountofNa+ reabsorptionoccursviatheNa+/H+ antiporter,thisresultsinanincreaseinH+ secretion(HCO3− reabsorption)bytheproximaltubule.InthissettingtheentirefilteredloadofHCO3− isreabsorbedandnewHCO3− generationmayevenbeenhanced.Thelatterresponseoccursbecausealdosterone,thelevelsofwhichareelevatedinvolumecontraction,notonlystimulatesdistalNa+ reabsorptionbutalsoH+ secretionbyintercalatedcells.ThisstimulationofH+ secretiongeneratesnewHCO3− byenhancingtitratableacidandNH4+ excretion.Thusinindividualswholosegastriccontents,metabolicalkalosisandparadoxicallyacidicurinecharacteristicallyoccur.Correctionofthealkalosisoccursonlywheneuvolemiaisreestablished.
Table 37.1 summarizes the primary alterations and the subsequent compensatory or defense mechanisms of the various simple acid-base disorders. In all acid-base disorders the compensatory response does not correct the underlying disorder but simply reduces the magnitude of the change in pH. Correction of the acid-base disorder requires treatment of its cause.
Types of Acid-Base Disorders
Metabolic acidosis is characterized by a decreased ECF [HCO3 −] and pH. It can develop via the addition of nonvolatile acid to the body (e.g., diabetic ketoacidosis), the loss of nonvolatile base (e.g., HCO3 − loss caused by diarrhea), or failure of the kidneys to excrete titratable acid and NH4 + (e.g., renal failure). As previously described, the buffering of H+ occurs in both the ECF and ICF compartments. When the pH falls, the respiratory centers are stimulated and the ventilatory rate is increased (respiratory compensation).
Finally, in metabolic acidosis, RNAE is increased. This occurs via elimination of all HCO3 − from urine (enhanced reabsorption of filtered HCO3 −) and via increased titratable acid and NH4 + excretion (enhanced production of new HCO3 −). If the process that initiated the acid-base disturbance is corrected, the enhanced RNAE will ultimately return the pH and [HCO3 −] to normal. After correction of the pH, the ventilatory rate also returns to normal.
Metabolic alkalosis is characterized by an increased ECF [HCO3 −] and pH. It can occur via the addition of nonvolatile base to the body (e.g., ingestion of antacids), as a result of volume contraction (e.g., hemorrhage), or more commonly from loss of nonvolatile acid (e.g., loss of gastric HCl because of prolonged vomiting). Buffering occurs predominantly in the ECF and to a lesser degree in the
Respiratoryacidosis↓ Respiratoryalkalosis↑ ECF,extracellularfluid;ICF,intracellularfluid;RNAE,renalnetacidexcretion